In 1994, I described rosacea as a cutaneous and ocular vascular disease,1 which was based on premises the most compelling of which was that patients with severe flushing due to systemic disease often had rapidly progressive rosacea, including ocular rosacea, facial telangiectasia, and phymatous changes. The earliest stages of rosacea were proposed to have an inflamed superficial vasculature and low-grade sterile superficial dermal cellulitis due to recognized provocative factors, such as local irritants, temperature extremes, wind, and flushing reactions. Subsequently, I have sought articles adding molecular details to my mental picture of this vascular pathogenesis of rosacea, and the evidentiary harvest has been abundant.